Fig. 1: Fructose mimics a metabolic profile akin to nutrient restriction.
From: Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation
A Seahorse extracellular flux analysis of ECAR in monocytes before and following injections of glucose, fructose, galactose (11.1 mM) or no sugar, LPS (10 ng/mL) and 2-DG (100 mM) at the time points indicated with average basal (Av. basal) and LPS-stimulated (Av. LPS) ECAR values. B Analysis of OCR in monocytes with the same injections as in panel (A), including average basal (Av. basal) and LPS-stimulated (Av. LPS) OCR values. C Change in ECAR (Δ ECAR) post 2-DG treatment. D Change in OCR (Δ OCR) post 2-DG treatment. E OCR versus ECAR map of average basal and LPS-stimulated values for glucose, fructose, galactose and no sugar treatment groups. Arrows indicate the shift in metabolism from average basal to average LPS. F Representative flow cytometry plot and DRAQ7 viability measurements of glucose, fructose, galactose and no sugar monocytes cultured for 24 h with LPS (10 ng/mL). Statistical significance was assessed using a one-way ANOVA with Dunnett’s (A–D) or Tukey’s (F) multiple comparisons test. Data are either representative of either three (A–E) or four independent experiments (F). Data are expressed as mean ± SEM; ***p ≤ 0.001. Source data are provided as a Source Data file.
